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At least 19 recordsLinked to original sources
PubMed1978

Pyridoxine and atherosclerosis: role of pyridoxine in the metabolism of lipids and glycosaminoglycans in rats fed normal and high fat, high cholesterol diets containing 16% casein.

The effect of administration of low and high doses of pyridoxine on the metabolism of lipids and glycosaminoglycans has been studied in rats fed normal and high fat, high cholesterol diets. Low doses of pyridoxine (0.005 mg/100 g body weight) caused increased concentrations, of cholesterol and triglycerides in the serum and aorta in animals fed normal and high fat, high cholesterol diets. Administration of high doses of pyridoxine (5.0 mg/100 g body weight) caused decrease in the concentration of these lipids in these tissues except in the case of the aorta in the animals fed a normal diet. Low doses of pyridoxine generally caused a decrease in the concentration of many glycosaminoglycan fractions in the aorta in rats fed normal and high fat, high cholesterol diets, whilst high doses caused an increase. The activity of glucosaminephosphate isomerase (glutamine-forming) and UDPglucose dehydrogenase, both key enzymes in the biosynthetic pathway of glycosaminoglycans, decreased in rats given low doses of pyridoxine and increased in rats given high doses. The activity of many enzymes concerned with degradation of glycosaminoglycans--hyaluronoglucosidase, beta-glucuronidase, beta-N-acetylglucosaminidase, aryl sulphatase, and cathepsin D--generally increased in rats fed low doses of the pyridoxine and decreased in those given high doses. The concentration of hepatic 3'-phosphoadenosine-5'-phosphosulphate, and the activity of the sulphate-activating system and of aryl sulphotransferase decreased when the dose of pyridoxine was low and increased when the dose was high.

Animals↗
PubMed1976

Effects of magnesium and high dietary intakes of pyridoxine on the chick.

Day-old broiler-type male chicks were used to determine what effects magnesium and high dietary pyridoxine had on the chick's performance. The chicks were randomly assigned to 15 treatments of magnesium at 875, 1375 and 1875 mg/kg. diet and pyridoxine at 1, 4, 31, 301, and 3001 mg/kg. diet in a 3 x 5 factorial block design. A regression was used to study some of the criteria. The highest mortality of 20% occurred in chicks on the 1875 mg. magnesium-3001 mg. pyridoxine treatment. Magnesium and pyridoxine had highly significant effects on body moisture. Effects due to magnesium and pyridoxine and the interaction between the two were highly significant for weight gain and the efficiency of feed utilization (E.F.U.) At 1875 mg. magnesium/kg diet, maximum growth response and E.F.U. were predicted to occur on 10 and 39 mg pyridoxine/kg diet, respectively, Neither magnesium nor the interaction between magnesium and pyridoxine had any significant effect on carcass protein. Pyridoxine had a highly significant effect on carcass protein. Maximum response in carcass protein occurred at 31 mg. pyridoxine/kg diet irrespective of magnesium level. Serum aminotransferase activity (S.A) was significant for magnesium, pyridoxine and the interaction between the two. Pyridoxine requirement for maximum S.A. was 49 mg/kg diet at 1875 mg magnesium/kg diet. Pyridoxine requirement for maximum response was highest for S.A. and least for growth. But S.A. had the highest R2 whereas growth had the least.

Animal Feed↗
PubMed1976

Mineral metabolism in chicks on high dietary pyridoxine and magnesium.

The effect of high dietary pyridoxine and magnesium on tissue electrolytes was studied in day-old broiler-type male chicks. There were 15 treatments of 875, 1375 and 1875 mg. magnesium/kg. diet and pyridoxine at 1, 4, 31, 301, 3001 mg./kg. diet in a 3 x 5 factorial block design. The sodium concentration of the liver decreased linearly with increasing dietary magnesium concentration expressed as log 10. In the kidney, no such effect was observed. The response of sodium concentration in these two tissues to increasing dietary pyridoxine, also expressed as log 10, was curvilinear, decreasing to minimum concentrations at pyridoxine intakes estimated to be equal to 40 mg./kg. of diet for the liver and 50 for the kidney and thereafter increasing. Potassium concentration of the liver exhibited opposite trends to those for sodium concentration but the responses to dietary magnesium were not consistent at each dietary pyridoxine concentration. Kidney potassium content followed essentially opposite trends to those of sodium. Kidney calcium decreased with increases in either dietary magnesium or pyridoxine, but the decreases were not consistent. The magnesium content of the kidney tended to increase with increases in dietary magnesium. Dietary pyridoxine resulted in a curvilinear response only in those chicks fed the 1875 mg. diet, decreasing to a minimum value at a pyridoxine intake of 26 mg., and increasing at higher pyridoxine dietary concentrations. No significant effects on sodium, potassium, calcium and magnesium concentrations in the heart were observed. It was speculated that the maximum potassium retention estimated to occur in the livers of birds consuming a diet containing 48 mg. pyridoxine/kg. diet might be due to increased glycogen turnover or increased phosphorylase activity.

Animals↗
PubMed1976

Influence of pyridoxine supplementation on vitamin B-6 levels in milk of rats deficient in the vitamin.

Levels of vitamin B-6 in milk from pyridoxine deficient dams were used as an indicator of the ability of pyridoxine to protect offspring against the effects of the deficiency. Sprague Dawley rats were fed a basal diet containing 30.0 (control) or 1.2 (deficient) mg pyridoxine-HC1/kg diet from weaning throughout growth, gestation and until 5 days postpartum. At this time, deficient dams were supplemented by a single intraperitoneal injection of 600 mug pyridoxine-HC1, or by adding 30 or 60 mg pyridoxine-HC1/kg to the diet. The vitamin B-6 content in milk form the group supplemented by injection exceeded the control level of 38.8 mug/100 ml milk 30 minutes after the injection, and reached a peak level of 110.7 mug/100 ml at 4 hours with a subsequent decline to 27mug/100 ml at 20 hours. In rats supplemented orally with 30 or 60 mg pyridoxine-HC1/kg diet, the vitamin B-6 level in the milk reached the control value in 24 and 6 hours, respectively. At 120 hours, orally supplemented dams had significantly higher levels of vitamin B-6 in the milk than control animals. Vitamin supplementation of dams by a single injection of pyridoxine-HC1 was sufficient to overcome the pyridoxine deficiency syndrome in the pups, but was not adequate for optimum growth.

Animals↗
PubMed1979

Interrelationship between dietary pyridoxine and free plasma amino acids in chicks.

The interrelationships between dietary pyridoxine and free plasma amino acids in young chicks were studied with two different diets. Chicks fed isolated soybean protein supplemented with less than 1.0 mg pyridoxine-HCl/kg diet had reduced body weight gain and feed consumption and a higher mortality rate (19%) than those fed 1 or 5 mg pyridoxine-HCl/kg. A casein diet required greater supplementation (2.0 mg pyridoxine/kg) to prevent reduced body weight gain and depressed feed intake. The concentrations of free plasma taurine, threonine, and serine were significantly lower in chicks fed the isolated soybean protein diet supplemented with less than 1.0 mg pyridoxine-HCl/kg, while those of isoleucine, valine, glycine, and ornithine were significantly higher than in chicks fed greater levels of pyridoxine. Supplementation of casein diets with less than 2.0 mg resulted in a significant accumulation of threonine, glycine, cystathionine, and ornithine. Valine was significant higher in chicks fed casein supplemented with only .6 mg pyridoxine-HCl/kg. Feeding isolated soybean protein or casein diets without any pyridoxine supplementation resulted in the dealth of 95% and 100% of the chicks, respectively. Pair feeding a group fed the isolated soybean protein diet supplemented with 1.0 mg to a group receiving .5 mg pyridoxine-HCl/kg resulted in a similar body weight gain and concentration of amino acids in the plasma.

Amino Acids↗
PubMed1976

Metabolism of pyridoxine in the liver of vitamin B-6-deficient rats.

The metabolism of [6-3H]pyridoxine - HCl was investigated in the liver of vitamin B-6-deficient rats. Rats were made vitamin B-6 deficient by feeding ad libitum for 42 days a diet lacking pyridoxine but otherwise optimal. Animals were each injected intraperitoneally with 33 muCi of [6-3H] pyridoxine - HCl and killed at different time intervals afterwards up to 7 days. Radioactively labeled hepatic B-6 compounds were extracted with acid and chromatographically separated on Dowex-X8 (H+) columns and the percent radioactivity for each vitamin compound was then calculated. Maximal uptake in control and deficient animals was observed 30 and 60 min, respectively, after administration of label. Radioactivity was not retained by the control animals but decreased steadily in a linear fashion after 30 min, reaching a low level after 3 h. On the other hand, vitamin deficient animals accumulated almost twice as much radioactivity in their liver as the controls and retained it through 7 days. In vitamin B-6 deficient animals 93% of the injected radioactivity was metabolized within 2 min at which time pyridoxine 5'-P and pyridoxal 5'-P reached 36 and 44% levels, respectively. Pyridoxine 5'-P dropped to minimal values (3%) within 15 min and remained unchanged for 7 days while pyridoxal 5'-P reached a peak (79%) level at 15 min and then began to drop linearly reaching a plateau (29%) at 5 days. Further, as the level of pyridoxal 5-P was falling, pyridoxamine 5'-P was linearly synthesized reaching a platuau low level (3%). The specific activity level of pyridoxal kinase decreased 3.2 times and that of pyridoxine 5'-phosphate oxidase increased 1.5 times in the state of deficiency. The results presented show that metabolism of [3H]pyridoxine in deficiency is characterized by (a) a delayed, two-fold increase in label uptake as well as an extended label retention period, (b) a rapid pyridoxal 5'-P synthesis, and (c) a continuous synthesis (and accumulation) of pyridoxamine 5'-P which is not utilized or further metabolized.

Aging↗
PubMed1976

Postnatal patterns of brain lipids in progeny of vitamin B-6 deficient rats before and after pyridoxine supplementation.

The influence of deficient and adequate maternal intakes of pyridoxine on lipid profiles in brains of progeny at 5, 10, 15, 25 and 50 days of age was studied. The effects of supplementing deficient dams at two different times with pyridoxine on the brain development of progeny were also examined. Three groups of weanling, female rats were fed diets deficient in pyridoxine (1.2 mg pyridoxine-HC1/kg diet) and another group received a control diet (30.0 mg pyridoxine-HC1/kg diet). One deficient group and the control group were fed their diets throughout growth, gestation and lactation. Two groups of dams were fed the deficient diet through growth, gestation and until 5 or 10 days postpartum when pyridoxine was supplemented by feeding the control diet. Body and brain weights were significantly lower in 15, 25 and 50 day-old progeny of deficient dams and deficient dams supplemented at 10 days postpartum. Cerebroside content at 15 days and ganglioside content at 15 and 25 days were significantly lower in brains of pups from unsupplemented deficient dams and deficient dams supplemented at 10 days postpartum. The postnatal development of cerebroside and ganglioside levels in brain was delayed or retarded in brain of pups from unsupplemented deficient dams. Supplementation of dams fed a low level of pyridoxine (1.2 mg/kg diet) with the vitamin beginning at 5 days postpartum reversed all observed effects of the low vitamin intake on brain lipids in progeny.

Age Factors↗
PubMed1976

Treatment of women with the galactorrhea-amenorrhea syndrome with pyridoxine (vitamin B6).

Three women with the galactorrhea-amenorrhea syndrome and elevated prolactin concentrations experienced a return of regular ovulatory menses within 37-94 days after starting pyridoxine treatment (200-600 mg/day). In each the galactorrhea ceased and serum prolactin levels were maintained in the normal range while taking pyridoxine. In two other women with prolonged secondary amenorrhea but without hyperprolactinemia or galactorrhea, pyridoxine at dosages up to 600 mg/day did not restore ovulatory menses. Pyridoxine treatment was also ineffective in decreasing profuse galactorrhea in one woman with normal prolactin levels and regular ovulatory menses. In the three women effectively treated with pyridoxine, the galactorrhea returned, serum prolactin levels increased, and the menses ceased after discontinuing pyridoxine. These results imply that pyridoxine, by decreasing the excessive secretion of prolactin, may be useful in the long-term medical management of women with hyperprolactinemia and the galactorrhea-amenorrhea syndrome.

Adult↗
PubMed1977

Uptake of pyridoxine hydrochloride by the rat jejunal mucosa in vitro.

The kinetics of mucosal membrane transport of pyridoxine hydrochloride were evaluated in vitro in the rat jejunum. Utilizing everted sacs and a double-label isotope technique, short-term incubation within the period of initial linear tissue uptake indicated: 1) no evidence of saturation of uptake over a wide pyridoxine-HCl concentration range (0.01 muM-10 mM); 2) failure of 4-deoxypyridoxine (10 muM), anoxia, iodoacetamide (5 mM), Na+ replacement and ouabain (1 mM) to inhibit uptake of 2 muM pyridoxine-HCl significantly; and 3) a low Q10 value of 1.31. Using single-label techniques, sacs were also incubated for 1 hour in 2 muM pyridoxine HCl with determination of the apparent tissue water-mucosal fluid concentration ratio and chromatographic separation of the various forms of vitamin B6 in tissue. Results demonstrated a failure of pyridoxine in tissue water to achieve a concentration in excess of that in the incubation medium. Data, therefore, were most consistent with passive diffusion as the mechanism for in vitro jejunal mucosal uptake of pyridoxine-HCl in the rat.

Animals↗
PubMed1979

Pyridoxine requirements of channel catfish.

In 20 and 12 week feeding trials, channel catfish fingerlings were fed purified diets containing five levels (0, 5, 10, 20, and 30 mg/kg) and six levels (0, 1, 2, 5, 10, and 20 mg/kg) of supplemental pyridoxine hydrochloride. Fish fed unsupplemented diets (pyridoxine content of 1.2 mg/kg) were characterized by anoxeria, nervous disorders, tetany, greenish-blue body coloration, and eventual mortality. Anemia, which has been reported in pyridoxine deficient salmonids, was not observed in pyridoxine deficient catfish. However, a microcytic, normochromic anemia was observed in groups fed high dietary levels of pyridoxine (20 mg/kg or greater). The dietary pyridoxine level required for maximal growth was approximately 3 mg/kg of diet. All other deficiency signs were prevented by 2.2 mg/kg of diet.

Animals↗
PubMed1979

Influence of dietary pyridoxine on selected immune capacities of rat dams and pups.

The influence of dietary pyridoxine on passive antibody transfer from dams to pups and on active humoral antibody formation by the pups was studied. Rats were fed diets containing 20.0, 0.6, 0.45, or 0.3 mg pyridoxine-HCl/kg during gestation and 20.0, 0.4, 0.3, or 0.2 mg/kg during lactation (diets A, B, C, and D). Diets B, C, and D contained 100, 75, and 50% of the NRC requirement for pyridoxine during gestation and lactation. After pups in groups B, C, and D developed signs of pyridoxine deficiency, all dams were fed diet A on days 9 to 21 of lactation. On day 9 vitamin B-6 levels were lower in spleens and thymuses of pups and in milk in groups B, C, and D. However, IgG in sera of dams and pups and in milk indicated that passive antibody transfer was similar for all groups. After weaning, pups in groups A, B, C, and D were fed diets containing 20.0, 0.4, 0.2, and 0 mg vitamin B-6/kg, respectively. On day 35 vitamin B-6 levels were lower in spleens and thymuses of pups fed inadequate pyridoxine (groups B, C, and D). These pups had fewer spleen cells and splenic antibody-forming cells (AFC) and lower levels of humoral antibody. The reduction in spleen cells and splenic AFC resulted in part from lower food intake but was intensified by pyridoxine deprivation.

Aging↗
PubMed1977

Effect of pyridoxine deficiency on cholesterogenesis in rats fed different levels of protein.

Hepatic cholesterol contents in rats fed a 70% or 20% casein diet with or without pyridoxine was determined. In the case of the 70% casein group, pyridoxine-deficient rats showed a higher content than the control. The increment was mainly due to the accumulation of an ester form of the cholesterol. On the other hand, pyridoxine-deficient rats in the 20% casein group showed a slightly lower content. The cholesterol content in liver microsomal fractions was lower in the 20% casein pyridoxine-deficient group and serum cholesterol level was lower in the 70%-casein pyridoxine-deficient group than those in respective control groups. Incorporation of [14C]acetate into cholesterol was studied using liver slices, and significant stimulation was observed in pyridoxine-deficient rat fed a 20% or 70% casein diet. There was no difference in intestinal cholesterogenesis between the control and the deficient groups.

Animals↗
PubMed1978

Pyridoxine and its relation to lipids. Studies with pyridoxineless mutants of Aspergillus nidulans.

The effect of pyridoxine deficiency on fat metabolism was studied using mutant strains of Aspergillus nidulans requiring pyridoxine for growth. Under pyridoxine deficiency the mutants exhibited increased levels of total lipid, sterols, phospholipids, and triacylglycerols. Total fatty acids were found to decrease with pyridoxine deficiency. An increase in saturated fatty acids and decrease in unsaturated fatty acids were seen with deficiency. Pyridoxine deficiency also increased lower carbon chain fatty acids. A possible involvement of pyridoxine in the elongation of fatty acid chain and in the desaturation of fatty acids in Aspergillus nidulans is suggested.

Aspergillus nidulans↗